After lunch, I have them put their dishes in the sink or dishwasher (ahem, if I’ve emptied it from the night before) then we mosey down the hall to get ready for naps. Naptime can be a struggle if your child isn’t “Buying In.” Here is how you can get your child
Cupro Skirt NEW CITY BRIGHT by VIDA VIDA Purchase 8UPFU46f1W
.

It doesn’t always happen at exactly 1, but 1 is the goal. This means by around this time all the kids are in their rooms with lights out to nap or, those who are old enough they don’t need a nap every day, have a few quiet activities they can play independently. My 5-year-old may only nap once a week, and my 4-year-old only 4 days a week or so.

4:00 pm | Wake up and snack

The time at which everyone wakes up varies. If my older kids aren’t napping they can come out of their rooms after a couple of hours and do something quiet. Or they often go into each other’s rooms to play quietly. Often all the nappers will sleep until 5:00 pm if I let them! I’ve found waking up cranky is remedied by a quick snack (not too filling or sweet).

We aim for eating between 5 and 5:30 pm. This is early, I know, but means we aren’t in a manic panic to do the wind down routine and the kids still get to bed at a reasonable hour. Reasonable being between 7 and 7:30 pm most nights. This works for our family.

6:00 pm | Bath and bedtime routine

If we haven’t swam that day then it’s usually bath time, books, pajamas, and calm play before bed. That said, kids will be kids and calm can turn to chaos quickly. My husband and I conquer and divide so each child can have a few minutes alone with each parent before bed. These
wind down routines
are key for babies, and I normally get baby duty. A mommy privilege!

Case 1:
A 33-year-old woman was in generally good health until she presented with acute-onset prolonged flu-like symptoms followed by hepatitis secondary to Epstein-Barr virus (EBV), significant weight loss, and recurrent fevers. She continued to develop intermittent fevers after discharge, and she was readmitted 11 months later for sepsis with EBV/cytomegalovirus viremia. She had no history of recurrent infections, and her family history was noncontributory. Her immune workup revealed pan-hypogammaglobulinemia (IgG <35 mg/dL, IgM <6 mg/dL, IgA <7 mg/dL), and she was given a diagnosis of CVID and started on IVIG.

It is important to emphasize that CVID is a diagnosis of exclusion and that other defined causes of hypogammaglobulinemia must be ruled out before making the diagnosis (
9
9.
Cunningham-Rundles C.
How I treat common variable immune deficiency. Blood. 2010;116:7-15. [PMID:
20332369
]
). This patient was given a diagnosis of CVID due to profoundly low immunoglobulin levels of multiple subtypes, but further immune studies also revealed CD4 lymphopenia of 113 cells/µL (normal range, 493 to 1,666 cells/µL), absent B cells, depressed NK cell function, and abnormal lymphocyte proliferation to mitogens. Although a small percentage of patients with CVID will have absent or low B lymphocytes, the additional findings are atypical of CVID and should prompt additional investigations. For instance, an underlying genetic defect such as in hemophagocytosis lymphohistiocytosis may have predisposed her to acquire an EBV infection and a secondary immunodeficiency.

Malignancy is another likely possibility. The patient's initial bone marrow biopsy was described as active EBV infection-associated bone marrow changes, although reevaluation was consistent with diffuse large B-cell lymphoma. Due to religious preferences, the patient declined a stem-cell transplant and succumbed to adenovirus septic shock within months.

Despite increasing numbers of individuals diagnosed with primary immune defects, secondary etiologies remain the leading cause of immunodeficiency in adults. Infectious diseases (HIV, CMV, EBV) and malignancy (B-cell malignancies, chronic lymphocytic leukemia, Good's syndrome, and non-Hodgkin lymphoma) are well-described causes of secondary hypogammaglobulinemia. Medication exposures can also be responsible. Glucocorticoids are by far the most common offending agent, although biologics, antimalarials, captopril, carbamazepine, gold salts, phenytoin, and other antiepileptics have also been implicated. Finally, systemic disorders that result in either hypercatabolism or increased loss of immunoglobulins, such as in protein-losing enteropathy, must also be ruled out (
10
10.
Conley ME, Notarangelo LD, Etzioni A.
Diagnostic criteria for primary immunodeficiencies. Representing PAGID (Pan-American Group for Immunodeficiency) and ESID (European Society for Immunodeficiencies). Clin Immunol. 1999;93:190-7. [PMID:
10600329
]
). In the case presented above, one must question why a healthy 33-year-old woman would suddenly develop a profound, combined immunodeficiency and disseminated EBV infection. Thus, malignancy is a more likely diagnosis.

cpc certification

Also, I did a blog post called CPT exam layout and
CPT exam tips
that I wanted to show you so if you go to coding certification.org on the sidebar there’s a search box that you can use to find, say Laureen and Alicia put in a post on this, that’s a good place to start and here is the little search box here. I just typed in layout because I knew that was what I had put in here and you will find the article. So basically, I’ve been doing this since 1999. I know basically what the main 15 categories are. I had also put this up on the AAPC discussion board and so go to this and you can see exactly what they are. Medical terminology, anatomy, practice management and coding guideline questions, and by the way, there are roughly ten of each of these, ten ICD-9 CM questions, HCPCS, ten EM, anesthesia, radiology, PAP and lab, medicine , ten from the 10,000 series so any code that starts with a 1 to a 6 is a surgery question.

So 10 from the integument surgery section, ten from musculoskeletal, ten from respiratory and cardio, ten from the 40,000 series, ten from the 50, ten from the 60. That’s roughly how it breaks down. So this is not available on the AAPC website so this should help you greatly and of course there are the three main CPC tips, take the course, like our 80 hour
medical coding course
, hint, hint, do a coding certification review class or videos like our review Blitz video and then 3. Practice, practice, practice. Make sure you take as many exams as you can possibly afford. Budget and time because you want to make sure are hitting 85% on a timed practice exam. I think this link actually takes you to another blog post. “Practice
CPC exam questions
I recommend”.

For the past 2-3 weeks, we have addressed the cardiovascular system. Its impossible to cover everything and that has never been our intention. Keep in mind that we are painting with a broad brush.

What is a Pacemaker?
This week’s tidbit is on
pacemakers
. A pacemaker is a small device that’s placed in the chest or abdomen to help control abnormal heart rhythms. This device uses low-energy electrical pulses to prompt the heart to beat at a normal rate.
Pacemakers
are used to treat arrhythmias
. Arrhythmias are problems with the rate or rhythm of the heartbeat (too slow, too fast, or irregular.)

Although it weighs just about an ounce, a pacemaker contains a powerful battery, electronic circuits, and computer memory that together generate electronic signals. The signals, or pacing pulses, are carried along thin, insulated wires, or leads, to the heart muscle. The signals cause the heart muscle to begin the contractions that cause a heartbeat. Simply stated, the pacemaker consists of two parts, the pacemaker itself or generator and the wires or leads.

Problem for this week: The patient, a 55-year-old woman, was seen by her doctor, complaining of shortness of breath, dizziness and fatigue. Her physician ordered a 12-lead EKG. After interpreting the results, she was diagnosed with bradycardia, a condition of the heart beating too slowly. This type of arrhythmia was complicated by tachycardia-bradycardia syndrome, aka sick sinus syndrome. She was admitted to the outpatient surgery setting for initial insertion of dual-chamber pacemaker, percutaneous approach, in the right atrium and the right ventricle. Code the diagnosis and ICD-10 procedures.

To locate 0JH636Z:
PCS Index > Pacemaker > Dual Chamber > Chest > 0JH6 > locate table 0JH and go across the row to finishing building the code after determining that the 4th character value of 6 is correct:

To locate 02H63JZ:
PCS Index > Insertion of device in > Atrium > Right > 02H6 > Locate table 02H and go across the row to finish building the code, making sure that the 4th character value of 6 is correct:

Insertion of Pacemaker into Right Atrium, Percutaneous Approach

To locate 02HK3JZ:
PCS Index > Insertion of device in > Ventricle > right > 02HK > locate table 02H and go across the row ensuring that the 4th character value of c 6 is correct:

Intramolecular hydrogen bonds found in a cellulose decasaccharide from a 5-ns simulation in the presence of explicit water molecules. (
a
) Shows all of the hydrogen bonds numbered in order of observation, irrespective of the type of interaction. (
b
) Shows the important interactions (A–C) found across the β(1→4) linkages of cellulose. (
c
) Shows the presence of the interactions detailed in (
b
) at each of the linkages in the decasaccharide and the molecular length as a function of time. Marked over this is the molecular length which would be predicted if the molecule took up a conformation as in the cellulose-I crystal.

Intramolecular hydrogen bonds found in a cellulose decasaccharide from a 5-ns simulation in the presence of explicit water molecules. (
a
) Shows all of the hydrogen bonds numbered in order of observation, irrespective of the type of interaction. (
b
) Shows the important interactions (A–C) found across the β(1→4) linkages of cellulose. (
c
) Shows the presence of the interactions detailed in (
b
) at each of the linkages in the decasaccharide and the molecular length as a function of time. Marked over this is the molecular length which would be predicted if the molecule took up a conformation as in the cellulose-I crystal.

The nature of these hydrogen bonds can be elucidated by separating them into categories. In the case of cellulose, three major intramolecular hydrogen-bonding interactions were observed, and these are labeled A, B, and C in
Figure 3b
. Their presence during the simulation, at each linkage, is detailed in
Figure 3c
. Hydrogen bond A corresponds to the localization of OH3 with respect to O5 and is predicted to be a particularly persistent interaction in the cellulose structure as seen in
Figure 3c
. The other two interactions involve the hydroxymethyl moiety; B represents the interaction from OH3 to O6, and C represents the interaction from OH6 to O3.

Observation of the molecular length as a function of time permits a visualization of the overall polymer dynamics. This parameter is documented from the simulation of a cellulose decasaccharide in
Figure 3c
. On this figure the predicted length for a decasaccharide based on the axial rise observed in the cellulose I crystal (
Gardner and Blackwell, 1974
) has been marked (5.15 nm) and is close to the maximum length obtainable for cellulose. The predicted dynamic length stayed close to this value for the majority of the cellulose simulation, although excursions to more contracted conformations (∼4.4 nm) were observed ephemerally. These excursions correspond to unusual conformations, and presumably water structure, at one or more of the polymer linkages, which last for only a few picoseconds. Thus the emergent average polymer conformation is highly extended and very close to that observed in crystal structures.